CFB MED03 Respiratory System
The respiratory system is the organ system responsible for gas exchange, conducting air through the airways to the alveoli where oxygen is absorbed into the blood and carbon dioxide is expelled from the body.
Respiratory System: Introduction — CFB (MED03) Comprehensive Exam-Ready Notes
This CFB lecture by Dr David CL Lam is your foundational framework for approaching any patient with a respiratory complaint. It answers three questions in sequence [1]:
- What is the patient complaining of? → History Taking (symptoms)
- What can you find on the patient? → Physical Examination (signs)
- What tests help you confirm/refine? → Investigations
Everything in respiratory medicine — from a simple cough to a life-threatening pulmonary embolism — is solved by rigorously applying these three steps. The lecture deliberately spans the full breadth of respiratory topics (symptoms, examination, investigations including lung function, ABG, imaging, bronchoscopy, polysomnography) because this is the map you will return to throughout clinical rotations and, critically, in your summative exams.
Learning Objectives (verbatim from slides) [1]:
- History taking for common symptoms of respiratory diseases: cough and sputum, haemoptysis, chest pain, and shortness of breath
- The principles of physical examination of the respiratory system (detecting physical signs)
- The common tests in the investigation of respiratory diseases
- Illustrative cases of patients presenting with respiratory symptoms — the clinical approach
"Patient comes to see you with a complaint of discomfort, i.e. with a symptom. You will take steps: to make the diagnosis (3 steps) → to manage." [1]
| Step | What You Do | What You Get |
|---|---|---|
| 1. History | Ask structured questions | Symptoms |
| 2. Physical Examination | Look, feel, listen on the patient | Signs |
| 3. Investigations | Order targeted tests | Objective data |
Why this matters: These three steps are sequential and complementary. History narrows the differential to 2–3 likely diagnoses. Examination refines it further. Investigations confirm and quantify. Examiners test whether you can do all three systematically — skipping straight to investigations is a classic mistake that loses marks.
2. History Taking — Detailed Breakdown
The structure is: Chief Complaint (+ duration) → HPI → Past Health → Personal/Social History (TOCC, smoking, alcohol) → Family History → Drug History [1]
| Component | Content | Why It Matters |
|---|---|---|
| Chief Complaint (CC) | One-liner + duration | Frames entire workup |
| HPI | About CC (character, severity, timing, aggravating/relieving), systemic enquiry, associations, progress, complications | Narrows the DDx |
| Past Health | Previous lung disease (TB, asthma), surgery, co-morbidities | Old TB → bronchiectasis, destroyed lung; DM → ↑infection risk |
| Personal/Social Hx | TOCC, smoking (pack-years), alcohol, occupation, allergy | Occupation links to silicosis, asbestosis; smoking to COPD/cancer; allergy history relevant to asthma/atopy |
| Family Hx | Asthma, atopy, lung cancer, alpha-1-antitrypsin deficiency | Genetic predisposition |
| Drug Hx | Medications causing respiratory effects | See drug table below |
HPI Example (from lecture) [1]
Mr ABC, M/70. CC: Haemoptysis for two days. HPI: 2 months — increased cough with scanty sputum; 2 weeks — increased shortness of breath; 2 days — blood in sputum.
This illustrative case teaches you to present the chronological evolution of symptoms — the earliest symptom first, then the progressive worsening, and finally the presenting complaint. In exams, marks are often given for showing the tempo of the disease.
The five major pulmonary symptoms are: Cough, Sputum, Haemoptysis, Dyspnoea, Chest Pain/Discomfort. [1]
High Yield: Five Major Pulmonary Symptoms
Whenever you are asked to "name respiratory symptoms," these five are the answer. They appear repeatedly in SAQ and minicase questions. [1, 7, 8]
Respiratory symptoms are divided into:
- Upper respiratory tract: nasal discharge/blockage, post-nasal drip
- Lower respiratory tract: cough, sputum, haemoptysis, dyspnoea, chest pain/discomfort
- Aerodigestive tract: reflux
- Systemic symptoms [1]
Systemic symptoms that may occur in association with a respiratory disease: Fever, Chills and rigors, Weight loss, Loss of appetite [1]
Why separate URT from LRT? Because the differential changes dramatically. Post-nasal drip is a common cause of chronic cough that mimics LRT disease. Reflux (GORD) can present as cough via vagal irritation of the lower oesophagus and microaspiration. Always ask about these — they are classic exam discriminators.
For all symptoms, assess [1]:
- Onset — acute or chronic
- Severity
- Timing of occurrence
- Associated factors and diseases
- Other associated symptoms
This five-point framework applies to every respiratory symptom and ensures systematic characterisation during history taking.
Cough & Sputum:
- Acute (days): Acute viral/bacterial URTI, Acute pneumonia, Asthma
- Subacute (weeks): TB, Lung cancer, Asthma
- Chronic (years): COPD, Bronchiectasis, Asthma [1]
Characterising the cough itself [1]:
- Productive or non-productive
- Type and quantity of sputum
- Time relations (e.g. nocturnal cough → asthma, GORD)
- Provoking factors (e.g. cold air, exercise)
- Associated features (e.g. wheeze, fever)
| Time Course | Differential Diagnoses | Key Discriminators |
|---|---|---|
| Acute (days) | URTI, pneumonia, asthma exacerbation | Fever → infective; wheeze → asthma |
| Subacute (weeks) | TB, lung cancer, asthma | Night sweats/weight loss → TB; haemoptysis + smoker → cancer |
| Chronic (years) | COPD, bronchiectasis, asthma | Smoking → COPD; copious purulent sputum → bronchiectasis; episodic/reversible → asthma |
Notice that asthma appears in all three categories — this is deliberate. Asthma can present acutely (exacerbation), subacutely (undiagnosed), or chronically (poorly controlled). This is an exam trap: don't pigeonhole asthma as only acute.
Acute dyspnoea causes: Asthma, Acute exacerbation of COPD, Pneumothorax (P), Pneumonia (P if pleuritis), Acute pulmonary oedema (P), Pulmonary embolism (P). P = with pain. [1]
Chronic (days/weeks): Pleural effusion, Pneumonia, Heart failure, Asthma.
Chronic (months/years): COPD, Asthma, Bronchiectasis, Restrictive lung diseases (pulmonary fibrosis, silicosis, kyphosis/scoliosis, destroyed lung by old TB), Heart failure. [1]
Exam Trap: 'P' Notation
The lecture marks certain causes with "P" = with pain. This means that in these conditions, the dyspnoea is typically accompanied by chest pain. This is a clinical discriminator: e.g., dyspnoea WITHOUT pain → think asthma/COPD; dyspnoea WITH pleuritic pain → think PE, pneumothorax, or pneumonia with pleuritis. Examiners love asking "which acute causes of dyspnoea are typically painful?" [1]
Common causes: Carcinoma of lung (P), Tuberculosis, Bronchiectasis, Acute tracheitis/bronchitis/necrotising pneumonia/lung abscess, Pulmonary embolism with infarct (P). P = with pain. [1]
Why these five? They represent the most important causes to rule out in any patient coughing up blood:
- Lung cancer — must be excluded in any smoker > 40 with haemoptysis; the "P" (pain) here refers specifically to pleura / thoracic cage metastasis [1]
- TB — Hong Kong has intermediate TB prevalence; always consider
- Bronchiectasis — recurrent infections cause vascular hypertrophy → haemoptysis
- Infection/abscess — necrotising organisms erode pulmonary vessels
- PE with infarction — lung tissue dies, vessels rupture
From past papers, haemoptysis with weight loss in a smoker = lung cancer until proven otherwise [7, 8, 9].
TOCC History — for ALL patients with fever and CXR consolidation:
- T = Travel
- O = Occupation
- C = Contact
- C = Cluster [1]
Why TOCC? This was formalised during SARS and reinforced during COVID-19. It identifies:
- Travel: endemic infections (avian flu from poultry farming, MERS from Middle East)
- Occupation: silicosis (construction workers), asbestosis (shipyard), farmer's lung
- Contact: known TB, COVID-19 close contacts
- Cluster: outbreak recognition (multiple cases in a family/workplace/ward)
The lecture specifically mentions SARS, Avian Flu, COVID-19 and the example of a poultry farmer (Avian flu) [1].
Drugs may cause:
- Worsening of asthma/COPD: Aspirin, Beta-blockers
- Increased infections (e.g. ↑ TB): Corticosteroids
- Diffuse lung shadows/fibrosis: Amiodarone [1]
| Drug | Respiratory Effect | Mechanism |
|---|---|---|
| Aspirin | Worsening asthma | Inhibits COX → shunts arachidonic acid to leukotriene pathway → bronchoconstriction (aspirin-exacerbated respiratory disease) |
| Beta-blockers | Worsening asthma/COPD | Block β2-receptors in bronchial smooth muscle → bronchoconstriction |
| Corticosteroids | ↑ TB, ↑ infections | Immunosuppression → reactivation of latent TB; impaired neutrophil/macrophage function |
| Amiodarone | Pulmonary fibrosis | Direct cytotoxic damage to pneumocytes; phospholipid accumulation → inflammation → fibrosis |
High Yield: Drug-Induced Respiratory Disease
These four drug-respiratory effect pairs are directly from the lecture slides and are commonly tested. If asked "name drugs that worsen asthma," answer aspirin and beta-blockers. If asked "name a drug causing pulmonary fibrosis," answer amiodarone. [1]
Other drugs that cause pulmonary fibrosis (from supporting material): methotrexate, bleomycin, nitrofurantoin [2, 5].
3. Physical Examination of the Respiratory System
GENERAL examination:
- Respiratory distress or not
- Fever
- Cyanosis
- Clubbing / tobacco staining
- (JVP)
- Oedema of legs: bilateral (cor pulmonale — RHF due to lung/pulmonary vascular disease), unilateral (DVT)
- Cervical / supraclavicular lymph nodes [1]
Breaking this down:
| Finding | What It Suggests | Clinical Reasoning |
|---|---|---|
| Respiratory distress | Severe/acute pathology | Use of accessory muscles, tachypnoea, inability to complete sentences |
| Fever | Infection (pneumonia, TB, abscess) | Must prompt TOCC |
| Cyanosis | Hypoxaemia (SaO2 < ~85%) | Central (tongue/lips) = low PaO2; peripheral = poor perfusion |
| Clubbing | See table below | Loss of Lovibond's angle → nail-bed fluctuation |
| Tobacco staining | Smoking history | Confirms exposure; correlates with COPD/cancer risk |
| JVP | Cor pulmonale, fluid overload, SVC obstruction | Raised + pulsatile = cor pulmonale; fixed/non-pulsatile = SVCO |
| Bilateral leg oedema | Cor pulmonale (RHF from lung disease) | Right heart fails because pulmonary hypertension ↑ afterload |
| Unilateral leg oedema | DVT → risk of PE | Asymmetric swelling is DVT until proven otherwise |
| Cervical/supraclavicular LNs | Metastatic lung cancer, lymphoma, TB | Supraclavicular = Virchow's node (left) — classic for thoracic/abdominal malignancy |
Pulmonary causes of clubbing:
- Lung cancer
- Suppurative lung diseases: Lung abscess, Bronchiectasis, Empyema thoracis
- Idiopathic lung fibrosis [1]
High Yield: Clubbing Causes (Pulmonary)
The mnemonic approach: L-A-B-E-F — Lung cancer, Abscess, Bronchiectasis, Empyema, Fibrosis. Examiners frequently ask "name causes of clubbing" — include cardiac (cyanotic congenital heart disease, infective endocarditis) and GI (cirrhosis, IBD) in addition to these pulmonary causes. [1]
Why does clubbing occur? The exact mechanism is debated, but the leading theory involves megakaryocytes and platelet clumps bypassing the pulmonary capillary filter (normally they fragment there). In lung disease, shunting or damaged capillary beds allow intact megakaryocytes to reach the fingertips where they release PDGF and VEGF, stimulating connective tissue growth. This is why conditions causing right-to-left shunting (cyanotic CHD) or chronic lung inflammation/destruction produce clubbing.
Chest examination: Inspection → Palpation → Percussion → Auscultation [1]
Inspection:
- Shape: barrel chest (hyperinflation in COPD/emphysema), kyphoscoliosis (restrictive defect) [1]
- Scars: VATS scars (small, 1–2 cm; minimally invasive thoracic surgery), standard thoracotomy scar (posterolateral, large) [1]
- Chest wall movement: symmetry, respiratory rate, pattern
- Scoliosis — specifically shown in lecture slides as a cause of restrictive lung disease [1]
Palpation:
- Tracheal position (midline vs deviated)
- Chest expansion (reduced on affected side)
- Tactile vocal fremitus
Percussion:
Percussion findings:
- Resonant → normal
- Dull → collapse, consolidation
- Stony dull → effusion
- Hyper-resonant → air (pneumothorax, emphysema) [1]
| Percussion Note | Pathology | Why |
|---|---|---|
| Resonant | Normal lung | Air-filled alveoli vibrate freely |
| Dull | Consolidation, collapse | Solid/airless lung tissue transmits sound poorly |
| Stony dull | Pleural effusion | Fluid completely dampens percussion vibrations — more dull than consolidation |
| Hyper-resonant | Pneumothorax, emphysema | Excessive air (trapped or free) amplifies vibration |
Auscultation:
Auscultation findings:
- Crackles: Coarse (bronchiectasis), Fine (fibrosis) [1]
| Sound | Character | Pathology | Mechanism |
|---|---|---|---|
| Coarse crackles | Low-pitched, early inspiratory, may clear with cough | Bronchiectasis, pneumonia | Air bubbling through secretions in dilated airways |
| Fine crackles | High-pitched, late inspiratory, "velcro" | Pulmonary fibrosis, early pulmonary oedema | Sudden opening of collapsed small airways/alveoli |
| Wheeze | Expiratory, polyphonic | Asthma, COPD | Narrowed airways vibrate during expiration |
| Bronchial breathing | Loud, high-pitched, equal inspiration/expiration | Consolidation | Sound transmitted efficiently through solid lung |
| Reduced/absent breath sounds | Quiet or silent | Effusion, pneumothorax, collapse | Sound blocked by fluid/air or no ventilation |
From 2024 MCQ [9]:
| Physical Sign | Most Likely Diagnosis |
|---|---|
| Wheezing during inspiration | Retrosternal goitre (extrathoracic upper airway obstruction) |
| Stony dull percussion note | Malignant pleural effusion |
| Bilateral fine basal crackles, JVP not raised | Idiopathic pulmonary fibrosis |
| Bronchial breath sound + increased vocal resonance | Pneumococcal pneumonia |
Exam Intelligence: Percussion Note Discriminator
"Stony dull" = effusion. "Dull" = consolidation or collapse. Examiners specifically test whether you can distinguish these. Consolidation has dullness PLUS bronchial breathing and increased vocal resonance (because solid lung transmits sound). Effusion has stony dullness PLUS reduced/absent breath sounds and reduced vocal resonance (because fluid blocks sound). [1, 9]
From the Respiratory Examination deck (James Ho, 2024) [3] and senior notes [4]:
- Pursed lip breathing: seen in COPD — creates auto-PEEP to keep small airways open
- Tracheal tug: accessory muscle use pulling trachea downward during inspiration — sign of severe airway obstruction
- Hoover's sign: paradoxical inward movement of lower rib cage during inspiration — hyperinflation in COPD
- Horner syndrome: miosis, ptosis, anhidrosis — Pancoast tumour invading sympathetic chain
- SVCO signs: facial/neck swelling, dilated veins over upper chest wall, fixed raised JVP — from 2022 minicase, this is a favourite exam scenario [7]
4. Investigations in Respiratory Disease
Common Respiratory Investigations: Blood, Sputum, NPA, Pleural fluid, Imaging, Lung function tests, ABG/Oximetry, Bronchoscopy, Lung FNA/biopsies, Polysomnography [1]
Blood tests:
- CBP — WBC: neutrophilia, eosinophilia
- Serology — infections (e.g. viral): paired samples for antibodies in 14 days; autoimmune vasculitic disease with pulmonary presentations (e.g. SLE, RA): ANF, ds-DNA, RF etc. [1]
| Test | What It Shows | Clinical Application |
|---|---|---|
| Neutrophilia | Bacterial infection | Pneumonia, lung abscess |
| Eosinophilia | Allergic/parasitic | Asthma, allergic bronchopulmonary aspergillosis (ABPA), eosinophilic pneumonia |
| Paired serology | Rising antibody titre confirms infection | Take acute + convalescent samples 14 days apart; 4-fold rise is diagnostic |
| Autoimmune markers | Connective tissue diseases affecting lungs | SLE (ANF, dsDNA) → pleural effusion, lupus pneumonitis; RA (RF) → ILD, pleural effusion |
Sputum examination:
- Gross appearance
- Amount
- Microscopy: Wright's stain (WBC), Gram's stain (bacteria), Ziehl-Neelsen stain (AFB/TB), Cytology (malignant cells)
- Culture: Aerobic, Anaerobic bacteria; Mycobacteria; Fungi
- Molecular testing ("quick" test): TB, viruses & others [1]
| Stain | Target | Diagnoses |
|---|---|---|
| Wright's stain | WBC types | Neutrophils = bacterial; eosinophils = asthma/allergy |
| Gram's stain | Bacteria morphology | Gram +ve diplococci = S. pneumoniae; Gram -ve rods = H. influenzae |
| Ziehl-Neelsen | Acid-fast bacilli | TB; requires 3 consecutive early morning sputum samples |
| Cytology | Malignant cells | Lung cancer — especially squamous cell (central) |
| Culture | Organism identification + sensitivities | Guides antibiotic therapy; mycobacterial culture takes 4–6 weeks |
| Molecular (PCR) | Rapid detection of DNA/RNA | TB GeneXpert (result in hours vs weeks); also for viruses |
Sputum characteristics as diagnostic clues (from supporting material [6]):
- Blood-streaked → TB, lung cancer
- Bloody mucopurulent → bronchiectasis, lung abscess
- Pink frothy → pulmonary oedema
- Rusty → pneumococcal pneumonia
- Copious purulent → bronchiectasis
NPA for: Influenza — molecular test detecting viral RNA; SARS/MERS/COVID-19 — molecular test detecting viral RNA [1]
NPA is preferred over sputum for upper respiratory viruses because the nasopharynx is the primary site of viral replication. Molecular tests (RT-PCR) detect viral RNA with high sensitivity and specificity, and are much faster than viral culture.
Pleural fluid examination:
- Appearance: clear/bloody/purulent/milky
- Chemistry: pH, protein, LDH
- Cell counts & differential
- Cytology
- Microbiology
- Others: e.g. adenosine deaminase (ADA) [1]
Light's Criteria (from supporting material — essential for exams [5, 6]):
An effusion is exudative if ANY ONE of these criteria is met:
- Pleural protein / serum protein > 0.5
- Pleural LDH / serum LDH > 0.6
- Pleural LDH > 2/3 upper limit of normal serum LDH
| Transudative | Exudative |
|---|---|
| Heart failure | Pneumonia (parapneumonic) |
| Cirrhosis | TB (high ADA > 40 U/L) |
| Nephrotic syndrome | Malignancy (positive cytology) |
| Hypoalbuminaemia | Empyema (purulent, pH < 7.2) |
High Yield: ADA in Pleural Fluid
The lecture specifically mentions ADA (adenosine deaminase). ADA > 40 U/L in lymphocytic exudative effusion is highly suggestive of TB pleuritis in endemic areas like Hong Kong. This is a favourite exam point. [1, 5]
Thoracentesis (Chest Tapping):
Chest tapping (thoracentesis) +/- Pleural biopsy (Abram's needle). Ultrasound guidance minimises bleeding and pneumothorax. [1]
Plain CXR: Note that masses in the mediastinum or behind the heart may be missed. [1]
CT (axial cuts): picking up small nodules not detected by plain CXR; picking up mediastinal lymph nodes and masses. [1]
| Modality | Strengths | Limitations |
|---|---|---|
| Plain CXR | Fast, cheap, widely available; shows consolidation, effusion, pneumothorax, masses | Misses small nodules, retrocardiac masses, mediastinal pathology |
| CT thorax | High sensitivity for nodules, masses, LNs, PE (with contrast) | Radiation, cost, contrast risk |
| CT pulmonary angiography | Gold standard for PE | Contrast allergy/renal impairment |
| PET-CT | Staging lung cancer (metabolically active tissue lights up) | Expensive, false +ve with inflammation |
4.6 Lung Function Tests
Lung Function Tests: PFR, Spirometry (FEV1/FVC), Lung Volumes (TLC, RV), Diffusing Capacity (DLCO), ABG (pH, PaO2, PaCO2), Oximetry (SaO2) [1]
The lecture beautifully organises these tests by what they measure:
- PFR and Spirometry → AIRWAY function
- DLCO → ALVEOLAR function
- ABG and Oximetry → DEFINING RESPIRATORY FAILURE [1]
A simple bedside test of large airway calibre. Most useful in asthma monitoring:
- Diurnal variation > 20% suggests asthma
- Serial PFR used to monitor response to treatment and identify triggers
FEV1 = Forced Expiratory Volume in 1 second; FVC = Forced Vital Capacity
FEV1/FVC ratio:
- Normal: > 70%, and both FEV1 & FVC normal
- Restrictive: ratio > 70%, but both FEV1 and FVC are low (e.g. fibrosis, kyphosis/scoliosis, pleural effusion)
- Obstructive: ratio < 70% [1]
| Pattern | FEV1/FVC | FEV1 | FVC | Examples |
|---|---|---|---|---|
| Normal | > 70% | Normal | Normal | Healthy |
| Obstructive | < 70% | ↓↓ | ↓ or normal | COPD, asthma |
| Restrictive | > 70% (or normal) | ↓ | ↓ | Pulmonary fibrosis, kyphoscoliosis, effusion |
Why FEV1/FVC < 70% = obstructive: In obstructive disease (asthma, COPD), the airways are narrowed or collapse during expiration. The patient can't blow air out quickly → FEV1 drops disproportionately more than FVC → ratio falls below 70%.
Why FEV1/FVC preserved in restrictive disease: In restrictive disease, the lungs are stiff or the chest wall can't expand. Both FEV1 and FVC are reduced proportionally because the total volume of air is reduced, but the airways themselves are not narrowed → ratio stays normal or even increases.
Exam Trap: Asthma vs COPD Spirometry
Both asthma and COPD show obstructive pattern (FEV1/FVC < 70%). The discriminator is reversibility: in asthma, FEV1 improves ≥ 12% AND ≥ 200 mL after bronchodilator. In COPD, there is minimal reversibility. The 2023 minicase tested this directly with pre- and post-bronchodilator spirometry values. [1, 8]
From the 2023 minicase (Mr Chan, construction worker, smoker, old TB) [8]:
- Pre-BD FEV1 = 1.20 L (60% predicted), FVC = 2.00 L (70%), FEV1/FVC = 60%
- Post-BD FEV1 = 1.25 L (62%), FVC = 2.10 L (71%)
- Interpretation: Obstructive pattern with NO significant reversibility → COPD (not asthma)
- This patient also had two respiratory diagnoses: COPD + bronchiectasis (or silicosis, given construction worker history)
DLCO measures the function of alveoli. Function of respiration is gaseous exchange (O2 and CO2). [1]
DLCO tests the efficiency of gas transfer across the alveolar-capillary membrane. The patient breathes a small amount of carbon monoxide (CO), which has very high haemoglobin affinity, so uptake is limited only by the membrane and capillary blood volume, not perfusion.
| DLCO | Condition | Why |
|---|---|---|
| ↓↓ | Pulmonary fibrosis | Thickened alveolar membrane impairs diffusion |
| ↓↓ | Emphysema | Destroyed alveolar surface area |
| ↓ | Anaemia | Less Hb to bind CO |
| ↑ | Pulmonary haemorrhage | Hb in alveoli binds CO → falsely high |
| ↑ | Polycythaemia | More Hb available |
Respiratory failure is logically defined by abnormal body O2/CO2:
- Low SaO2 / PaO2 = oxygenation failure (Type I)
- Low PaO2 + high PaCO2 = ventilatory failure (Type II) [1]
| Type | PaO2 | PaCO2 | Mechanism | Examples |
|---|---|---|---|---|
| Type I | Low (< 8 kPa) | Normal or low | V/Q mismatch, diffusion impairment, shunt | Pneumonia, PE, ARDS, ILD |
| Type II | Low (< 8 kPa) | High (> 6 kPa) | Alveolar hypoventilation | COPD exacerbation, neuromuscular disease, chest wall disease, drug overdose |
Why does Type I have normal/low CO2? Because CO2 diffuses 20× faster than O2 across the alveolar membrane. In V/Q mismatch, hyperventilation of well-ventilated areas compensates for CO2 elimination but cannot fully compensate for O2 (due to the shape of the oxyhaemoglobin dissociation curve — the flat upper portion means hyperventilation adds minimal extra O2 to already-saturated blood).
Why does Type II have high CO2? Because the problem is ventilation itself — the patient cannot move enough air in and out of the lungs, so both O2 delivery AND CO2 removal are impaired.
From the 2023 minicase ABG question [8]:
- pH 7.28, PaO2 8.0 kPa, PaCO2 7.0 kPa, HCO3 35 mmol/L, BE -6
- Interpretation: Type II respiratory failure (low PaO2 + high PaCO2) with partially compensated respiratory acidosis (pH still acidic but HCO3 elevated indicating chronic renal compensation)
- Management: NIPPV (non-invasive positive pressure ventilation) or invasive mechanical ventilation [8]
Pulse oximetry: SaO2 & pulse rate, non-invasive, continuous & real-time. ABG: pH, PaO2, PaCO2, bicarbonate (much more complete acid-base picture), invasive, not continuous/real-time. [1]
SaO₂ — Definition and Key Reference Values [1]:
- PaO₂ 13 kPa → SaO₂ ≈ 97% (normal)
- PaO₂ 8 kPa → SaO₂ ≈ 90% (threshold for respiratory failure)
These two reference points anchor the flat upper portion and steep middle portion of the oxyhaemoglobin dissociation curve, respectively.
| Feature | Pulse Oximetry | ABG |
|---|---|---|
| Parameters | SaO2, pulse rate | pH, PaO2, PaCO2, HCO3, BE, lactate |
| Invasiveness | Non-invasive (clip on finger) | Invasive (arterial puncture — radial/femoral) |
| Continuous | Yes | No (single time-point) |
| When to use | Screening, monitoring | Suspected respiratory failure, acid-base derangement |
| Limitations | Can't assess CO2 or acid-base; unreliable in poor perfusion, nail polish, CO poisoning | Painful, risk of haematoma, single snapshot |
High Yield: When to Order ABG vs Oximetry
If SaO2 is normal on oximetry and you just need monitoring → oximetry is sufficient. If you suspect Type II respiratory failure (e.g. drowsy COPD patient), you must get an ABG because oximetry cannot tell you the PaCO2. The 2023 minicase specifically tested ABG interpretation in a COPD patient. [1, 8]
Flexible bronchoscopy: allows viewing of airways, biopsy (forceps for tissue), brushing (cells for cytology), bronchoalveolar lavage. [1]
Indications:
- Suspected lung cancer (central lesions) → endobronchial biopsy
- Haemoptysis of unknown cause
- Suspected TB (sputum smear negative) → bronchoalveolar lavage (BAL) for AFB
- Suspected infection in immunocompromised patients
- Foreign body removal
- Airway assessment (strictures, fistulae)
Yield: Bronchoscopy is best for central lesions (visible endobronchially). For peripheral lesions, CT-guided transthoracic fine needle aspiration/biopsy is preferred [1].
Transthoracic FNA/biopsies under imaging guidance for peripheral lung lesions. [1]
When to use: Peripheral lung nodule/mass not reachable by bronchoscope. CT-guided to ensure accurate targeting. Main complication: pneumothorax (10–25% get a small pneumothorax; ~5% need a chest drain).
Polysomnography records body functions during sleep: brain electrical activity, respiratory effort, air flow, blood oxygen levels (SaO2). Used to diagnose sleep apnoea and determine its severity. Patient stays overnight in Sleep Lab. Home sleep study with simplified recordings is a recent development. [1]
Obstructive Sleep Apnoea (OSA) is characterised by repetitive upper airway collapse during sleep → apnoeas/hypopnoeas → desaturations → arousals → daytime somnolence. Polysomnography quantifies the Apnoea-Hypopnoea Index (AHI):
- Mild: AHI 5–15
- Moderate: AHI 15–30
- Severe: AHI > 30
Treatment: CPAP (continuous positive airway pressure) — essentially acts as a pneumatic splint to keep the upper airway open.
5. Illustrative Test Questions from the Lecture
"What are the three major symptoms of acute pulmonary thromboembolism with infarct?"
Answer:
- Dyspnoea (acute onset, often at rest)
- Pleuritic chest pain (sharp, worsened by inspiration — from infarcted lung tissue irritating pleura)
- Haemoptysis (blood from infarcted lung tissue)
"Describe the clinical features of a patient with bronchiectasis."
Answer:
- Symptoms: Chronic productive cough with copious purulent sputum (often postural — worse on lying down), recurrent chest infections, haemoptysis
- Signs: Clubbing, coarse crackles (persistent, may change with coughing), possible cyanosis in advanced disease
- Investigations: HRCT thorax (gold standard — shows signet ring sign, tram tracks, dilated airways); sputum culture (often Pseudomonas aeruginosa in established disease)
High Yield Summary
-
The respiratory clinical approach is: History → Examination → Investigations → Diagnosis → Management.
-
History
- Five major symptoms (cough, sputum, haemoptysis, dyspnoea, chest pain). Always get TOCC (Travel, Occupation, Contact, Cluster). Drug history is critical: aspirin/beta-blockers worsen asthma; corticosteroids reactivate TB; amiodarone causes fibrosis.
-
Examination
- General (distress, cyanosis, clubbing, oedema — bilateral = cor pulmonale, unilateral = DVT, cervical LNs).
- Chest: Inspection (scars, shape, symmetry) → Palpation (expansion, trachea) → Percussion (resonant = normal, dull = consolidation/collapse, stony dull = effusion, hyper-resonant = pneumothorax) → Auscultation (coarse crackles = bronchiectasis, fine crackles = fibrosis, wheeze = obstruction, bronchial breathing = consolidation).
-
Investigations
- Blood (CBP, serology), Sputum (Gram, ZN, culture, cytology, PCR), NPA (viral molecular tests), Pleural fluid (Light's criteria, ADA), Imaging (CXR — may miss retrocardiac/mediastinal lesions; CT for nodules/LNs), Lung function (PFR/Spirometry → airway; DLCO → alveoli; ABG/oximetry → respiratory failure), Bronchoscopy (central lesions), CT-guided biopsy (peripheral lesions), Polysomnography (OSA).
-
Respiratory failure
- Type I = low PaO2, normal/low PaCO2 (oxygenation failure). Type II = low PaO2 + high PaCO2 (ventilatory failure).
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Spirometry
- Obstructive = FEV1/FVC < 70%. Restrictive = FEV1/FVC ≥ 70% but both values low.
Active Recall - Respiratory System Introduction
[1] Lecture slides: CFB (MED03) Respiratory System.pdf (all pages cited throughout) [2] Senior notes: Maksim Medicine Notes.pdf (Respiratory medicine section, p. 295–302) [3] Lecture slides: Respiratory Examination for CFB_James Ho_2024.pdf (p. 1) [4] Senior notes: Ryan Ho Respiratory.pdf (p. 3–4) [5] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Chapter 2 Respiratory, p. 3) [6] Senior notes: learning_points_output.txt (Respiratory sections) [7] Past papers: 2022 Fourth Summative SAQ.pdf (Q2, Q6); 2022 Fourth Summative Minicase.pdf (Case 3) [8] Past papers: 2023 Fourth Summative Minicase.pdf (Case 1, Sections 2–4) [9] Past papers: 2024 Fourth Summative MCQ.pdf (Section B, Q1–4)
CFB MED11 Rehabilitation Medicine
Rehabilitation medicine is a medical specialty focused on restoring functional ability and quality of life in individuals with physical impairments or disabilities resulting from injury, illness, or chronic conditions.
CFB MED10 The Use Of Laboratory Test In Clinical Medicine
The systematic application of laboratory investigations—including selection, interpretation, sensitivity, specificity, and predictive values—to aid in disease screening, diagnosis, monitoring, and prognosis in clinical practice.